NEOSTRIATAL MODULATION OF MOTOR CORTEX EXCITABILITY

The influence of the basal ganglia motor loop on motor cortex function was examined by pharmacologically altering neostriatal activity while monitoring the electrical stimulation thresholds for eliciting movements of the ipsilateral and contralateral motor cortex in ketamine anesthetized rats. Repeated unilateral intraneostriatal infusions (1-3) of the glutamate agonist, kainic acid (0.1 mu l, 75 ng), or glutamate (0.3 mu l, 1.65 mu g) reliably increased ipsilateral but not contralateral cortical thresholds. Single infusions of kainic acid (0.3 mu l, 150 or 225 ng) elevated ipsilateral cortical thresholds for 30-45 min; with glutamate (0.3 mu l, 1.65 mu g), the change lasted less than 10 min. Antidromically identified striatonigral projection neurons (n = 8) located approximately 500 mu M from the infusion cannula, showed either increased firing (n = 4) for less than 10 min following glutamate infusion or no change from their non-firing state (n = 4). Non-antidromically activated neurons (n = 3) were all excited by the infusion, although an interval of inhibition preceded or followed the excitation in two cases. Infusions (0.3 mu l) of inhibitory agents (GABA, 31 and 310 ng; muscimol 34.2 ng; and DNQX 34.2 ng) did not alter cortical threshold, nor did saline vehicle. Lesion of the ventrolateral but not ventromedial thalamic nucleus prevented the modulation of cortical thresholds following intraneostriatal infusion of 225 ng kainic acid. Thus the neostriatal alteration of cortical thresholds indicates a modulation of cortical excitability via thalamic projections and not the outcome of competing descending cortical and neostriatal influences converging on motorneurons. These results suggest that tonic feedforward modulation of the motor cortex and the pyramidal tract by the basal ganglia can be inhibitory.